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91.
大豆甙元(S86019)与乳香有效成分Bc-4或阿糖胞苷对HL-60细胞分化的联合诱导 总被引:4,自引:0,他引:4
大豆甙元($86019)单独处理HL-60细胞,对细胞生长诱导分化作用较弱,NBT阳性细胞数低于10%。当S86019与乳香有效成分Bc-4联合应用时,对HL-60细胞的生长有明显抑制,并有明显的分化诱导;S86019与Bc-4或Ara-c联合应用,对细胞的增殖有较强的抑制和分化诱导作用。S86019与Bc-4联合应用4d,NBT阳性细胞达80%,75%细胞获得吞噬乳胶颗粒能力,90%细胞向成熟粒细胞方向分化;S86019与Ara-c联合应用4d,NBT阳性反应细胞达70%,82%细胞获得吞噬能力,90%细胞形态发生分化。S86019与Bc-4或Ara-c联合用药4d,可明显阻断细胞由G1期向s期移行,G1期细胞数明显增加。 相似文献
92.
The cell cycle perturbation effect on leukemic cells of the Brown Norway myelocytic leukemia (BNML) after high dose Ara-C injection was used as the rationale for chemotherapy studies. A one log leukemic cell load reduction as determined by means of the leukemic colony forming units-spleen (LCFU-S) assay was observed when the second Ara-C injection was administered during a period of induced accumulation of cells in S phase. Evidence was obtained that Ara-C was also cytotoxic for G1, phase cells. By comparing a continuous Ara-C infusion during 24 h with two Ara-C injections at the same total dosage given 12 h apart, it was found that the tumor load was significantly more reduced in the latter group. For the drug combination Ara-C/Adriamycin, maximal LCFU-S reduction of one log was observed when Adriamycin (7.7 mg/kg) was given 12 h after Ara-C. From the increase in survival time after the schedule of 6 × Ara-C plus 1 × Adriamycin (all injections given at 12 h intervals), it could be extrapolated that the tumor load was reduced by 6.7 logs; this was in agreement with the theoretically expected reduction of 6.2 logs based on the LCFU-S experiments. The schedule of 6 × Ara-C plus 1 × Adriamycin reduced the normal haemopoietic stem cell compartment by 2.5 logs. This therapeutic gain is attributed to the specific recruitment-synchronization inducing effect of Ara-C on leukemic cells in the G0 phase. 相似文献
93.
It has been suggested that the FLAG remission induction regimen comprising fludarabine (F-ara), cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (G-CSF) may be capable of overcoming P-glycoprotein (P-gp)-related multidrug resistance (MDR) in patients with acute myeloblastic leukaemia (AML). We have investigated the in vitro response of P-gp-positive and -negative AML clones to FLAG and compared this with their response to treatment with Ara-C and daunorubicin (DNR). Twenty-four cryopreserved samples from patients with AML were studied using a flow cytometric technique for the enumeration of viable (7-amino actinomycin D negative) cells. Samples consisted of 12 P-gp-positive and 12 P-gp-negative cases, as measured by the MRK16 antibody. The results were analysed by calculating the comparative drug resistance (CDR), i.e. the percentage cell death caused by Ara-C + DNR subtracted from the percentage cell death, caused by FLAG after 48 h incubation in suspension culture. P-gp-positive clones were shown to have a significantly higher CDR than P-gp-negative clones (P = 0. 001). Furthermore, a significant positive correlation (r2 = 0.40, P < 0.01) was found between P-gp protein expression and CDR. However, P-gp function, measured using cyclosporin modulation of rhodamine 123 (R123) uptake, was not associated with the CDR, demonstrating that there are other properties of P-gp, besides its role in drug efflux, that modulate the responsiveness of AML blasts to chemotherapy. These results are consistent with a potential benefit for FLAG in P-gp-positive AML, but not P-gp-negative AML, compared with standard anthracycline and Ara-C therapy. 相似文献
94.
95.
Due to the limited clinical experience there is no standard treatment of primary CNS-lymphomas (PCNSL). Based on the actual data it seems that high-dose methotrexate (HTMRX) and high-dose cytarabine (ARA-C) qualify as treatments of choice for this disease. The role of radiation therapy is still unclear, due to the high long-term toxicity, especially in elderly patients. We treated 14 HIV negative patients with 4–5 cycles of methotrexate (MTX) at 3500 mg/m2 and MTX 15 mg intrathecal weekly or MTX 8000 mg/m2 weekly without intrathecal treatment. Younger patients (< 60 y) received 3 weeks after last MTX dose a whole-brain irradiation (45 Gy + 9 Gy boost), older patientsts were not irradiated and continued CT. The following treatment consisted in ARA-C 3000 mg/m2 d1 + 2 every 3 weeks for two cycles. All patients received steroids for two months or until the end of radiotherapy. The overall response rate was 100%, 12/14 CR (86%). Two patients died still on treatment but not due to lymphoma (1 pulmonary embolism, 1 herpes encephalitis). Toxicity was very mild with no grade 3–4 non-haematological toxic events and almost 100% grade 3–4 leucopenia without episodes of neutropenic fever. After a median follow up of 39 months the PFS and OS are 65% (9/14) and 78% (11/14) respectively, and compare well with other trial results. 相似文献
96.
阿糖胞苷诱导HL-60细胞凋亡及其机制研究 总被引:2,自引:1,他引:2
为了研究阿糖胞苷诱导HL-60细胞凋亡及其机制,采用Giemsa染色、光学显微镜下观察HL60细胞的形态学变化,琼脂糖凝胶电泳检测DNA凋亡带,细胞免疫组织化学方法检测细胞凋亡相关基因Bcl-2、Bax的蛋白表达。结果显示:实验组自培养8小时起,细胞开始变形,Giemsa染色可见核膜裂解,染色质呈紫红色或蓝紫色,出现典型的凋亡小体;DNA凝胶电泳见典型的梯形条带;在细胞凋亡的同时伴有Bcl-2蛋白表达明显下降,而Bax蛋白表达明显升高,Bcl-2/Bax比值下降。结论:阿糖胞苷可明显地诱导HL60细胞凋亡,同时伴有Bcl乏蛋白表达降低、Bax蛋白升高。Bcl-2/Bax比值下降可能是阿糖胞苷诱导HL-60细胞凋亡的主要机制之一。 相似文献
97.
为探讨人类ERMAP基因在红细胞分化发育过程中的作用,本研究设计ERMAP—dsDNA,制备ERMAP—shRNA表达质粒,并建立稳定表达ERMAP—shRNA的K562细胞系(即ERMAP—shRNA/K562细胞系),观察Ara-C诱导ERMAP—shRNA/K562细胞向红细胞系分化过程中,细胞形态、联苯胺染色细胞阳性率和细胞表面标记等的变化,同时以FQ—PCR检测K562细胞人类ERMAP基因表达量的变化。结果发现:经Ara-C诱导72小时,ERMAP—shRNA/K562细胞与对照组比较,体积较大,胞浆量较少,着色大部分呈深蓝色或蓝紫色,部分细胞仍可见1—2个核仁;联苯胺染色阳性率由1.17%增加至2.04%(P〈0.05),但仍低于Ara—C诱导K562组(P〈0.05);CD36^-/CD235a^+细胞比例从8.83%增至11.28%,CD36^+/CD235a^+细胞比例从1.23%增至2.64%,CD36^+/CD235a^-细胞比例从0.59%增至1.47%,均明显低于Ara—C诱导K562细胞组;与此同时,ERMAP—shRNA/K562细胞ERMAP基因的表达量从诱导前的2.52×10^-3缓慢增加至诱导72小时后的4.53×10^-3,明显低于K562细胞组。结论:ER—MAP—shRNA可抑制Ara—C诱导K562细胞向红系分化的过程,这进一步提示人类ERMAP基因与红细胞分化发育过程有关。 相似文献
98.
目的 探讨阿糖胞苷对抗CD3/抗P-gP双功能抗体介导的T淋巴细胞免疫杀伤多药耐药白血病细胞的影响.方法 采用抗E-tag亲和层析柱分离纯化抗CD3/抗P-gp微型双功能抗体,用阿糖胞苷刺激K562和K562/A02细胞,并用流式细胞术检测K562和K562/A02细胞B7-1、B7-2分子的表达,用CytoTox 96非放射性细胞毒试剂盒检测阿精胞苷对抗CD3/抗P-gp双功能抗体介导的T淋巴细胞免疫杀伤K562/A02细胞的影响.结果 经阿糖胞苷刺激的K562和K562/A02细胞B7-1、B7-2分子的表达较未刺激的对照组明显升高.阿糖胞苷对抗CD3/抗P-gp双功能抗体介导的T淋巴细胞在效靶比0.39:1~25:1范围内,激活T细胞对耐药白血病细胞的杀伤率为(16.44±1.20)%~(60.49 ± 2.90)%,其杀伤率与效靶比和抗体浓度呈依赖关系(P<0.05).结论 阿糖胞苷可明显提高抗CD3/抗P-gp双功能抗体介导的人T淋巴细胞对高表达P-gp抗原的耐药白血病细胞的杀伤效应. 相似文献
99.
目的 探讨阿糖胞苷(Ara-C)在原代大鼠海马神经元早期纯化培养中的优化方法。 方法 新生1d SD大鼠海马神经元原代培养48 h后,不同浓度(0、2.5、5.0、7.5、10 mmol/L)Ara-C 处理0、6、12、24 h,光镜下观察细胞形态,采用MTT检测细胞活性,并通过细胞形态学分析神经元纯度,筛选出最优纯化浓度与时间;采用免疫荧光及Western blot技术检测微管相关蛋白2(MAP2)进一步检测神经元纯度,台盼蓝染色分析神经元存活率。 结果 大鼠原代海马神经元培养48 h,5 mmol/L Ara-C处理24 h得到的神经元纯度及活性最佳;MAP2免疫荧光染色结果显示,Ara-C处理组神经元纯度为(74.28±10.13) %,显著高于对照组(34.82±8.15)% (P=0.000);Western Blot结果显示Ara-C处理组MAP2蛋白水平显著高于对照组(P=0.008);台盼蓝染色显示Ara-C处理组与对照组间海马神经元存活率无差异,分别为(93.2±3.82)%和(95.6±2.37)% (P=0.109)。 结论 在大鼠原代海马神经元的早期培养过程中,5 mmol/L Ara-C处理24 h得到的海马神经元的纯度与活性最佳。 相似文献
100.